Micro Pharm Flashcards

1
Q

Difference between peniciliin G and V.

A

G = IV and IM. V = oral. pharmacology micro

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1
Q

Penicillin(mechanism,use,toxicity)

A

Bind penicillin-binding proteins(transpeptidases), block cross linking of peptidoglycans;most effective on G+, also N. Meningitidis, Treponema;hypersensitivy reaction, hemolytic anema. pharmacology micro

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2
Q

Oxacillin,Naficillin,Dicloxacillin(mechanism,use,toxicity)

A

bind transpeptidases, penicillanse resistant due to bukly r-group blocking B-Lactamse; S. Aureus, except MRSA; hypersensitivity and interstitial nephritis. pharmacology micro

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3
Q

Ampicillin, amoxicillin(mecanism,use,toxicity)

A

bind transpeptidases, wide spectrum and more penicillinase sensitive. combo with claculanic acid to protect from B-lactams;kills enterococci(HELPSS)H.iB, E.coli,Listera,Proteus,Salmonella,Shigella,enterococci;hypersensitivity reaction,rash,pseudomemrane colitis. pharmacology micro

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4
Q

Which has better bioavailibility; amoxicllin or ampicillin?

A

amOxicllin has better Oral bioavilability. pharmacology micro

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5
Q

What does clavulanic acid do?

A

B-lactamse inhibitor pharmacology micro

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6
Q

Ticarcillin,piperacillin(mechanism,use,toxicity)

A

transpeptidase inhibitor but extended spectrum;pseduomonas and g- rods, use with claculanic acid due to B-lactamse suspectibilty; hypersensitivity reaction. pharmacology micro

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7
Q

List the B-lactamse inhibitors

A

(CAST) Clavulanic Acid, Sulbactam,Tazobactem. pharmacology micro

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8
Q

Cephalosporin(mechanism,use,toxiciity)

A

inhibit cell wall synthesis but are less susceptible to B-lactamases, are bactericidal;use depends on generation, there are four;hypersensitivty reactions, vitamin K defiency, increased nephrotoxicity of aminoglycosides. pharmacology micro

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9
Q

give use of cefazolin, cephalexin.

A

1st generation cephalosporins. PEcK. Proteus, E.coli,Klebsiella. Cefazolin used preop to prevent A.aureus infections. pharmacology micro

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10
Q

give use of cefoxitin, cefaclor,cefuroxime`

A

2nd generation cephalosporins. HEN PEcKs. H.ib, Enterbacter, Neisseria, Proteus, E.coli,Klebsiella, Serratia. pharmacology micro

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11
Q

give use of ceftriaxone, cefotaxime,ceftazidime

A

3rd gen. cephalosporins. Serious gram - infections. Ceftriaxone = meningitis and gonorrhea. Ceftazidime = pseudomonas. pharmacology micro

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12
Q

give use of cefepime.

A

increased activity against pseudomonas and G+ bugs. pharmacology micro

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13
Q

Aztreonam(mechanism,use,toxicty)

A

a monobactem resistant to B-lactamases, prevents binding to PBP3 and is synergistic with aminoglycosides;gram - rods only;very nontoxic, some GI upset. pharmacology micro

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14
Q

what transpeptidase inhibitor can be used in penicillin allergy?

A

aztreonam. pharmacology micro

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15
Q

imipenem/cilastatin,meropenem,etrapenem,doripenem(mechanism,use,toxicity)

A

broad spectrum, B-lactamase resistent but imipenem needs cilastatin to inhibit renal dehydropeptidase. later carbepenems do not;G+ cocci,G- rods, anerobes. used only in life threating events;skin rash, CNS toxicity, seizures. pharmacology micro

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16
Q

Vancomycin(mechanism,use,toxicty)

A

inhibits cell wall binding peptidoglycan formation by binding D-ala percursors, is bacterialcidal; G+ only, especially for multidrug resistant onces;NOT - nephrotoxicity, ototoxicity, thrombophlebitis, red man syndrome. pharmacology micro

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17
Q

How is redman syndrome prevented in vancomycin use?

A

slow infusion and rate and antihistamines. pharmacology micro

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18
Q

How does vancomycin resistant occur?

A

amino acid change of D-ala D-ala to D-ala D-lac. pharmacology micro

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19
Q

List antibiotic protein synthesis inhibitors

A

AT 30, CCEL at 50. 30S = Aminoglycosides, Tetracyclines. 50S = Chloramphenicol, Clindamycin, Erythromycin, Linezolid. pharmacology micro

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20
Q

Gentamicin, neomycin, amikacin,tobramycin,streptomycin(mechanism,use,toxicity)

A

aminoglycosides, bacterialcidal, block translocation but require oxygen for uptake;ineffective in anaerobes,use in gram - rod infections and before bowel surgery; nephrotoxicty, NMJ block, ototoxicity, teratogen. pharmacology micro

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21
Q

how does resistenace to aminoglycosides occur?

A

transferase enzymes that inactivate the drug by acetylation, phosphorylation, or adenylation. pharmacology micro

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22
Q

tetracycline, doxycycline, demecycline,minocycline(mechanism, use, toxicity)

A

bacteriostatic, prevents aminoacyl-tRNA binds;Borrela, M. Pneuomo, Rickettsia, Chlamysia; can’t take with milk, antacids, iron because ions bind it, GI distress, discoloration of teeth, inhibition of bone growth, contraindication in pregnancy. pharmacology micro

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23
Q

how does resistance to tetracyclines occur?

A

decrease uptake into cells or increased efflux by pumps. pharmacology micro

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24
Azithromycin, clarithromycin, erythromycin(mechanism,use,toxicity)
bacteriostatic, blocks translocation; atypical pneumonias, chlamydia, gram + cocci; MACRO: increased Motility, arrhythmia, Cholestatic hepatitis, Rash, eOsinophilia. pharmacology micro
25
how does resitance to macrolides occur?
methylation of 23s rRNA binding site. pharmacology micro
26
Chloramphenicol(mechanism,use,toxicity)
Bacterialstatic, blocks peptidlytransferase; Meningitis in adults, used in power countries due to being cheap; dose dependent anemia, dose independent aplastic anemia, gray baby syndrome. pharmacology micro
27
what causes grey baby syndrome?
use of chloramphenicol in premature infants, they lack UDO-glucuronyl-transferase. pharmacology micro
28
How does resistance to chloramphenicol occur?
plasmid-encoded acetyltransferase. pharmacology micro
29
clindamycin(mechanism,use,toxicity)
Bacteriostatic. Blocks peptide transfer; anaerobic infections in lung infections and oral anerobes; C. Diff infection, fever, diarrhea. pharmacology micro
30
Sulfamethoxazole(SMX), sulfisoxazole, sulfadiazine(mechanism, use, toxicity)
Bacteriostatic, PABA metabolites inhibit dihydropteroate synthase; Gram +, G-, Nocardia, Chlamydia, UTI; hypersensitivty, hemolysis in G6PD, nephrotoxic, kernicterus, displaces other drugs from albumin. pharmacology micro
31
how does resistance to sulfonamides occur?
altered bacterial dihydropteroate or increased PABA synthesis. pharmacology micro
32
Trimethoprim(mechanism,use,toxicity)
Bacteriostatic, inhibits bacterial dihydrofolate reductase, blocks folate synthesis; used in UTI, PCP (prophylacis and treatment), shigella, salmonella; megaloblastic anemia, leukopenia, granulocytopenia. pharmacology micro
33
ciprofloxacin, norfloxacin, levofloxacin, etc...(mechanism, use, toxicity)
bactericidal, inhibits DNA gyrase(topo II and IV);G- rods of urinary and GI tracts, Neisseria, some G+;( lones hurt the bones) tenonitis and tendon rupture, superinfections, don't give to kids or pregnant women due to cartilage damage. pharmacology micro
34
how does resistance to fluroquinolones occur?
mutation in DNA gyrase or efflux pumps. pharmacology micro
35
What groups are susceptible to fluorquinolone tendon rupture?
older than 60 or taking prednisone pharmacology micro
36
Metronidazole(mechanism, use, toxicity)
bacterialcidal, forms free radical toxic metabolites that damge bacterial DNA damage; (GET GAP) Giardia, Entamoeba, trichomonas, Gardnerella, Anaerobes, Pylori; causes disulfiram like reaction, headache, metallic taste. pharmacology micro
37
Isoniazid(mechanism,use,toxicity)
decrease synthesis of mycolic acids, bacterial catalase peroxidase(KatG) must activate INH; TB drug, only one used as prophylaxis and in latent TB; peripheral neuropathy, hepatoxic, lupis like drug interaction, pyridoxine antagonist. pharmacology micro
38
Rifampin(mechanism,use,toxicity)
inhibits DNA-dependent RNA polymerase; TB, Leprosy, prophylaxis in meningococcus and Hib type B; hepatotox, p450 inducer, orange body fluids. pharmacology micro
39
Pyrazinamide(mechanism, use, toxicity)
unknown; TB; hyperuricemia, hepatotoxic. pharmacology micro
40
Ethambutol(mechanism,use,toxicity)
decreased carbohydrate polymerization of TB cell wall, blocks arabinosyltransferase; TB; optic neuropathy(red-green color blindness\_ pharmacology micro
41
Amphotericin B(mechanism, use, toxicity)
binds fungal ergosterol, causes holes in membranes; use in systemtic and CNS mycoses infections; fever/chills, hypotension, arrythmias, nephrotoxic, IV phlebitis, must supplement K and MG. pharmacology micro
42
nystatin(mechanism,use,toxicty)
binds fungal ergosterol;topical only due to high toxicity, used for oral thrush and topical diaper rash or vaginal candidiasis. pharmacology micro
43
Fluconazole, ketoconazole, clotrimazole, itraconazole, voriconazole(mechanism, use,toxicity)
inhibits fungal ergosterol synthesis by binding p450;Fluconazole for suppression of cryptococcus in AIDs patients, itraconazle for blasto, coccio, histo. pharmacology micro
44
Flucytosine(mechanism, use, toxicity)
inhibits fungal DNA and RNA synthesis by conversion to 5FU; used in systemic fungal infections, especially cryptococcus; bone marrow suppression. pharmacology micro
45
Caspofungin, micafungin(mechanism, use, toxicity)
inhibits fungal cell wall synthesis by inhibiting B-glucan synthesis; invasive aspergillosis, candida; flushing via histamine releae. pharmacology micro
46
terbinafine(mechanism,use,toxicity)
inhibits fungal squalene epoxidase; treat dermatophytes - toe nail infection especially;abnormal LFT, visual disturbances. pharmacology micro
47
Griseofulvin(mechanism,use,toxicity)
interferes with microtubules, stops mitosis in fungi;deposits in keratin so used in superficial infections, stops dermatophytes; teratogenic, carcinogenic, confusion, p450 inducer. pharmacology micro
48
Pyrimethamine use
toxoplasmosis pharmacology micro
49
suramin and melarsoprol use
trypanosoma brucei pharmacology micro
50
nifurtimox use
trypanosoma cruzi pharmacology micro
51
sodium stibogluconate use
leshmaniasis pharmacology micro
52
Chloroquine(mechanism,use,toxicity)
blocks formation of heme into hemozoin. Heme accumulates and is toxic to plasmodia;used on all species but falciparum(too much resitance); retinopathy pharmacology micro
53
quinidine use
lifethreatening malaria pharmacology micro
54
artemether/lumifantrine use
p. falciparum killing pharmacology micro
55
Zanamivir,oseltamivir(mechanism,use)
inihibits influenza neuraminidase, stops progeny release; treamt of influenze a and b pharmacology micro
56
Ribavarin(mechanism,use,toxicity)
inhibits sythesis of guanine nucleotides by competitvely inhibiting IMP dehydrogenase; RSV, chronic hep C; hemolytic anemia, severe teratogen pharmacology micro
57
Acyclovir,valacyclovir(mechanism, use, toxicity)
Guanosine analog, inhibits viral DNA polymerase; monophosphorylated by thymidine kinase in HSV/VZV so active in lesions and encephalitis, good for prophylaxis, pharmacology micro
58
Famciclovir use
used in herpes zoster active infections pharmacology micro
59
mechanism for resistance to acyclovir
mutated viral thymidine kinase pharmacology micro
60
Ganciclovir,valgangciclovir(mechanism,use,toxicity)
guanosine analog, 5'-monophosphate formed by CMV viral kinase, inhibits viral DNA polymerase;CMV infections;leukopenia,neutopenia,thrombocytopenia,renal toxicity pharmacology micro
61
mechanism for resistance to acyclovir
mutated CMV DNA polymerase or lack of viral kinase pharmacology micro
62
Foscarnet(mechanism,use,toxicity)
viral DNA polymerase inhibitor, binds to pyrofosphate binding site, doesn't need viral kinase activation;CMV retinitis when ganciclovir fails and acyclovir restitant HSV; nephrotoxic pharmacology micro
63
mechanism for resistance to foscarnet
mutated DNA polymerase pharmacology micro
64
cidofovir(mechanism,use,toxicity)
inhibits DNA polymerase, doesn't require activiation by viral kinase; CMV retenitis, acyclovir resistant HSV; nephrotoxic pharmacology micro
65
HAART consist of what?
[2 NRTI] +[1 NNRTI OR 1 protease inhibitor OR 1 integrase inhibitor] pharmacology micro
66
give mechanism and toxicity of protease inhibitors
all end in -NAVIR! stops HIV mRNA cleavage into functional parts; hyperglycemia, GI upset, lipodystrophy. pharmacology micro
67
Ritonavir does what to be a "booster"
inhibits cytochrome p-450, boosting concentration of other drugs. pharmacology micro
68
Tenofovir, emtricitabine, abacavir, lamivudine, zidovudine, didansoine, stavudine(mechanism,use,toxicity
(NRTI)competitively blocks binding of nucleotide to reverse transcriptase, only tenofovir doesn't need to be activated;all NRTIs, zidovidine used in pregnancy to reduce fetal transmision; bone marrow suppression, lactic acidosis, peripheral neuropathy. pharmacology micro
69
Nevirapine, Efavirenz, Delavirdine(mechanism,use,toxicity)
(NNRTI) bind at a site different from NRTIs, no don't require activation don't compete with nucleotides; bonow marrow suppression, peripheral neuropathy, lactic acidosis, pharmacology micro
70
Raltegravir(mechanism,use,toxicity)
inhibits integrase, which stops HIV integration into host cells;HIV;hypercholesterolemia pharmacology micro
71
Interferons(mechanism,use,toxicity)
glycoproteins synthesized my virus infected cells, block RNA and DNA virus replication; INFa- chronic hep b and c, Kaposi sarcoma, IFN-b -MS, INF-gamma -NADPH oxidase defiency; neutropenia, myopathy. pharmacology micro
72
What antibiotics must be avoided in pregnancy?
SAFe Children Take Really Good Care. sulfonamides(kericterus), aminoglycosides(ototox), fluoroquinolones(cartilage damage), Clarithromycin(embryotoxic), Tetracycline(teeth,bone damage),Ribavarin(teratogenic),Griseofulvin(teratogenic),Chloramphenicol(grey baby) pharmacology micro